Intracoronary stent implantation is a mechanical procedure, the success of which depends to a large degree on the mechanical properties of each vessel component involved and the pressure applied to the balloon. Little is known about the influence of plaque composition on arterial overstretching and the subsequent injury to the vessel wall following stenting. An idealised finite element model was developed to investigate the influence of both plaque types (hypercellular, hypocellular and calcified) and stent inflation pressures (9, 12 and 15 atm) on vessel and plaque stresses during the implantation of a balloon expandable coronary stent into an idealised stenosed artery. The plaque type was found to have a significant influence on the stresses induced within the artery during stenting. Higher stresses were predicted in the artery wall for cellular plaques, while the stiffer calcified plaque appeared to play a protective role by reducing the levels of stress within the arterial tissue for a given inflation pressure. Higher pressures can be applied to calcified plaques with a lower risk of arterial vascular injury which may reduce the stimulus for in-stent restenosis. Results also suggest that the risk of plaque rupture, and any subsequent thrombosis due to platelet deposition at the fissure, is greater for calcified plaques with low fracture stresses.

The effectiveness of a cardiovascular stent depends on many factors, such as its ability to sustain the compression applied by the vessel wall, minimal longitudinal contraction when it is expanded, and its ability to flex when navigating tortuous blood vessels. The long-term reaction of the tissue to the stent is also device dependant; in particular some designs provoke in-stent restenosis (i.e., regrowth of the occlusion around the stent). The mechanism of restenosis is thought to involve injury or damage to the vessel wall due to the high stresses generated around the stent when it expands. Because of this, the deflection of the tissue between the struts of the stent (called prolapse or “draping”) has been used as a measure of the potential of a stent to cause restenosis. In this paper, uniaxial and biaxial experiments on human femoral artery and porcine aortic vascular tissue are used to develop a hyperelastic constitutive model of vascular tissue suitable for implementation in finite-element analysis. To analyze prolapse, four stent designs (BeStent 2, Medtronic AVE; NIROYAL, Boston Scientific; VELOCITY, Cordis; TETRA, Guidant) were expanded in vitro to determine their repeating-unit dimensions. This geometric data was used to generate a finite element model of the vascular tissue supported within a repeating-unit of the stent. Under a pressure of 450 mm Hg (representing the radial compression of the vessel wall), maximum radial deflection of 0.253 mm, 0.279 mm, 0.348 mm and 0.48 mm were calculated for each of the four stents. Stresses in the vascular wall were highest for the VELOCITY stent. The method is proposed as a way to compare stents relative to their potential for restenosis and as a basis for a biomechanical design of a stent repeating-unit that would minimize restenosis.